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Journal articles on the topic 'DNA Damage; Drug effects; Genetics'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Araújo, Maria Cristina P., Francisca da Luz Dias, Andréa O. Cecchi, Lusânia M. G. Antunes, and Catarina S. Takahashi. "Chromosome damage induced by DNA topoisomerase II inhibitors combined with g-radiation in vitro." Genetics and Molecular Biology 21, no. 3 (1998): 407–17. http://dx.doi.org/10.1590/s1415-47571998000300021.

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Combined radiation and antineoplastic drug treatment have important applications in cancer therapy. In the present work, an evaluation was made of two known topoisomerase II inhibitors, doxorubicin (DXR) and mitoxantrone (MXN), with g-radiation. The effects of DXR or MXN on g-radiation-induced chromosome aberrations in Chinese hamster ovary (CHO) cells were analyzed. Two concentrations of each drug, 0.5 and 1.0 µg/ml DXR, and 0.02 and 0.04 µg/ml MXN, were applied in combination with two doses of g-radiation (20 and 40 cGy). A significant potentiating effect on chromosomal aberrations was obser

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2

Błasiak, J., and J. Kowalik. "Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate." Acta Biochimica Polonica 48, no. 1 (2001): 233–40. http://dx.doi.org/10.18388/abp.2001_5131.

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Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing secondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since human diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, conjugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lymphocytes was examined using the trypan blue exclusion test and the alk

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Tempel, Karlheinz, Hannelore Kortenbeutel, and Christina von Zallinger. "Bleomycin - Induced DNA Damage and DNA Repair in Chicken Embryo Cells as Compared to X-Irradiation." Zeitschrift für Naturforschung C 54, no. 12 (1999): 1068–74. http://dx.doi.org/10.1515/znc-1999-1211.

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Following in vitro- and in ovo-exposure of chicken embryo cells, the level of bleomycin (BM) - induced damage was evaluated by using DNA synthesis, nucleoid sedimentation (SED), and viscometry of alkaline cell lysates (VISC). This damage was compared to Xirradiation, using 5.9-378 nM BM in vitro, 1.5-116 μg BM/egg in ovo, and 2-32 Gy, respectively, in vitro as well as in ovo. With respect to BM. the most notable result is the increase in DNA synthesis and VISC at the lowest concentrations of the drug. A decrease in both parameters was observed at high BM concentrations and following exposure t

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Nemeth, Margit A., T. C. Hsu, and S. Pathak. "Chromosome instability in the murine melanoma cell line K-1735 is due to drug-specific mechanisms." Genetics and Molecular Biology 23, no. 4 (2000): 763–69. http://dx.doi.org/10.1590/s1415-47572000000400010.

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The purpose of the present study was to investigate chromosomal instability and DNA repair by exposing clones from the murine melanoma cell line K-1735 to the radiomimetic drug bleomycin and to the DNA polymerase a inhibitor aphidicolin. Results from previous experiments conducted with human lymphocytes have suggested synergistic chromosomal damage after simultaneous exposure to these two agents. However, in the murine cell line studied here, there was no direct correlation between the effects of these two agents. Indeed, the extensive variation in the responses to aphidicolin and bleomycin su

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Blasiak, Janusz, Kinga Widera, and Tomasz Pertyński. "Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells." Acta Biochimica Polonica 50, no. 1 (2003): 191–95. http://dx.doi.org/10.18388/abp.2003_3726.

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Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37 degrees C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 microM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37 degrees C or

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Szikriszt, Bernadett, Ádám Póti, Eszter Németh, Nnennaya Kanu, Charles Swanton, and Dávid Szüts. "A comparative analysis of the mutagenicity of platinum-containing chemotherapeutic agents reveals direct and indirect mutagenic mechanisms." Mutagenesis 36, no. 1 (2021): 75–86. http://dx.doi.org/10.1093/mutage/geab005.

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Abstract Platinum-based drugs are a mainstay of cancer chemotherapy. However, their mutagenic effect can increase tumour heterogeneity, contribute to the evolution of treatment resistance and also induce secondary malignancies. We coupled whole genome sequencing with phenotypic investigations on two cell line models to compare the magnitude and examine the mechanism of mutagenicity of cisplatin, carboplatin and oxaliplatin. Cisplatin induced significantly more base substitution mutations than carboplatin or oxaliplatin when used at equitoxic concentrations on human TK6 or chicken DT40 cells, a

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Gloc, Ewa, Mariusz Warszawski, Wojciech Młynarski, et al. "TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine." Acta Biochimica Polonica 49, no. 1 (2002): 121–28. http://dx.doi.org/10.18388/abp.2002_3828.

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The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13)) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. We investigated the ef

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Donmez-Altuntas, Hamiyet, Fahri Bayram, Ayse N. Coskun-Demirkalp, Osman Baspınar, Derya Kocer, and Peter P. Toth. "Therapeutic effects of statins on chromosomal DNA damage of dyslipidemic patients." Experimental Biology and Medicine 244, no. 13 (2019): 1089–95. http://dx.doi.org/10.1177/1535370219871895.

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Statins are a group of cholesterol lowering drugs and frequently used in the therapy of dyslipidemia. Our knowledge of the impact of statin therapy on DNA damage is as yet rudimentary. In this study, we aimed to assess the possible (1) genotoxic, cytostatic, and cytotoxic effects of statins in peripheral blood lymphocytes by using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay, and (2) oxidative DNA damage by measuring plasma 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels in response to statin therapy. Thirty patients with dyslipidemia who had no chronic diseases and did not use any m

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9

Mollazadeh, Samaneh, Maryam M. Matin, Ahmad Reza Bahrami, et al. "Feselol Enhances the Cytotoxicity and DNA Damage Induced by Cisplatin in 5637 Cells." Zeitschrift für Naturforschung C 66, no. 11-12 (2011): 555–61. http://dx.doi.org/10.1515/znc-2011-11-1204.

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Transitional cell carcinoma (TCC), which is the most common type of bladder cancer, shows resistance to chemotherapeutic agents due to the overexpression of drug efflux pumps. In this study, the effects of feselol, a sesquiterpene coumarin extracted from Ferula badrakema, on cisplatin cytotoxicity were investigated in 5637 cells, a TCC subline. Cell viability and DNA lesion were evaluated by thiazolyl blue tetrazolium bromide and comet assays, respectively. Feselol had no significant cytotoxic effect in 5637 cells but at 32 μg/mL it increased the cytotoxicity of 1 μg/mL cisplatin by 37% after

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Chen, Ling, Ting Zhang, Qiuli Liu, et al. "Buformin increases radiosensitivity in cervical cancer cells via cell-cycle arrest and delayed DNA-damage repair." Experimental Biology and Medicine 243, no. 14 (2018): 1133–40. http://dx.doi.org/10.1177/1535370218813320.

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Buformin is a commonly used hypoglycemic agent, and numerous studies have shown that buformin has potent antitumor effects in several malignancies. In this study, we aimed to assess the cytotoxic effect of buformin combined with ionizing radiation (IR) on two human cervical cancer cell lines (Hela and Siha). Cytotoxicity was detected by colony formation assays; impacts on the cell cycle and apoptosis were detected by flow cytometric analyses. Changes in histone H2AX (γ-H2AX) phosphorylation and impacts on the AMPK/S6 pathway were also explored. Our data show that the combination of buformin an

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Thomas, Adam M., Carrie Hui, Adam South, and Mitch McVey. "Common Variants of Drosophila melanogaster Cyp6d2 Cause Camptothecin Sensitivity and Synergize With Loss of Brca2." G3 Genes|Genomes|Genetics 3, no. 1 (2013): 91–99. http://dx.doi.org/10.1534/g3.112.003996.

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Abstract Many chemotherapeutic agents selectively target rapidly dividing cells, including cancer cells, by causing DNA damage that leads to genome instability and cell death. We used Drosophila melanogaster to study how mutations in key DNA repair genes affect an organism’s response to chemotherapeutic drugs. In this study, we focused on camptothecin and its derivatives, topotecan and irinotecan, which are type I topoisomerase inhibitors that create DNA double-strand breaks in rapidly dividing cells. Here, we describe two polymorphisms in Drosophila Cyp6d2 that result in extreme sensitivity t

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12

Sanomachi, Tomomi, Shuhei Suzuki, Keita Togashi, et al. "Spironolactone, a Classic Potassium-Sparing Diuretic, Reduces Survivin Expression and Chemosensitizes Cancer Cells to Non-DNA-Damaging Anticancer Drugs." Cancers 11, no. 10 (2019): 1550. http://dx.doi.org/10.3390/cancers11101550.

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Spironolactone, a classical diuretic drug, is used to treat tumor-associated complications in cancer patients. Spironolactone was recently reported to exert anti-cancer effects by suppressing DNA damage repair. However, it currently remains unclear whether spironolactone exerts combinational effects with non-DNA-damaging anti-cancer drugs, such as gemcitabine and epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Using the cancer cells of lung cancer, pancreatic cancer, and glioblastoma, the combinational effects of spironolactone with gemcitabine and osimertinib, a third

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Błasiak, Janusz, Ewa Gloc, and Mariusz Warszawski. "A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone." Acta Biochimica Polonica 49, no. 1 (2002): 145–55. http://dx.doi.org/10.18388/abp.2002_3831.

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Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assaywe showed that the drugs at 0.01-10 microM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 microM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produ

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14

Ferjani, Hanen, Rim Timoumi, Ines Amara, et al. "Beneficial effects of mycophenolate mofetil on cardiotoxicity induced by tacrolimus in wistar rats." Experimental Biology and Medicine 242, no. 4 (2016): 448–55. http://dx.doi.org/10.1177/1535370215616709.

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The immunosuppressive drug tacrolimus (TAC) is used clinically to reduce the rejection rate in transplant patients. TAC has contributed to an increased prevalence of cardiovascular disease in patients receiving solid organ transplantation. Mycophenolate mofetil (MMF), a potent inhibitor of de novo purine synthesis, is known to prevent ongoing rejection in combination with TAC. In the present study, we investigated the antioxidant and antigenotoxic effect of MMF on TAC-induced cardiotoxicity in rats. Oral administration of TAC at 2.4, 24, and 60 mg/kg b.w. corresponding, respectively, to 1, 10,

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Arora, Shagun, Chanderdeep Tandon, and Simran Tandon. "Evaluation of the Cytotoxic Effects of CAM Therapies: AnIn VitroStudy in Normal Kidney Cell Lines." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/452892.

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The purpose of this current study was to justify the incorporation of complementary and alternate medicine (CAM) in current cancer treatments. The major drawback of anticancer drugs is their nonselective killing, which ultimately leads to attrition of normal cells. Keeping this as the foundation of our study, we made an effort to compare the cytotoxicity associated with a known chemotherapeutic drug 5-Fluorouracil (5-FU), with certain CAM therapies previously reported to have anticancer activity. The parameters chosen for the study were based on antiproliferative and cytotoxic effects on norma

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Guerrero, Erika N., Joy Mitra, Haibo Wang, et al. "Amyotrophic lateral sclerosis-associated TDP-43 mutation Q331K prevents nuclear translocation of XRCC4-DNA ligase 4 complex and is linked to genome damage-mediated neuronal apoptosis." Human Molecular Genetics 28, no. 15 (2019): 2459–76. http://dx.doi.org/10.1093/hmg/ddz062.

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Abstract Dominant mutations in the RNA/DNA-binding protein TDP-43 have been linked to amyotrophic lateral sclerosis (ALS). Here, we screened genomic DNA extracted from spinal cord specimens of sporadic ALS patients for mutations in the TARDBP gene and identified a patient specimen with previously reported Q331K mutation. The patient spinal cord tissue with Q331K mutation showed accumulation of higher levels of DNA strand breaks and the DNA double-strand break (DSB) marker γH2AX, compared to age-matched controls, suggesting a role of the Q331K mutation in genome-damage accumulation. Using condi

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Corban, Monika, Mark Ambrose, Joanne Pagnon, et al. "Pathway Analysis of Fucoidan Activity Using a Yeast Gene Deletion Library Screen." Marine Drugs 17, no. 1 (2019): 54. http://dx.doi.org/10.3390/md17010054.

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Fucoidan, the sulfated fucose-rich polysaccharide derived from brown macroalgae, was reported to display some anti-cancer effects in in vitro and in vivo models that included apoptosis and cell cycle arrest. The proposed mechanisms of action involve enhanced immune surveillance and direct pro-apoptotic effects via the activation of cell signaling pathways that remain largely uncharacterized. This study aimed to identify cellular pathways influenced by fucoidan using an unbiased genetic approach to generate additional insights into the anti-cancer effects of fucoidan. Drug–gene interactions of

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Islam, Muhammad Torequl, Cristina Quispe, Mohammad S. Mubarak, et al. "Protective Effects of Natural Products and Their Derivatives on Genetic Material: A Critical Review." Records of Natural Products 15, no. 6 (2021): 433–62. http://dx.doi.org/10.25135/rnp.228.20.11.1871.

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Although treatment with natural products and the substances derived from them has gained much attention, it is important to know the genomic safety of these substances prior to their use in humans. The present review aims to present the current knowledge on the genoprotective effects and possible mechanism of actions of natural compounds. Therefore, an up-to-date search was conducted using known databases such as PubMed, ScienceDirect, and Clinicaltrials.gov. For the investigation of genotoxic/genoprotective activity of these substances, comet or micronucleus assay were frequently used models

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Babukov, Yordan, Radoslav Aleksandrov, Aneliya Ivanova, Aleksandar Atemin, and Stoyno Stoynov. "DNArepairK: An Interactive Database for Exploring the Impact of Anticancer Drugs onto the Dynamics of DNA Repair Proteins." Biomedicines 9, no. 9 (2021): 1238. http://dx.doi.org/10.3390/biomedicines9091238.

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Cells are constantly exposed to numerous mutagens that produce diverse types of DNA lesions. Eukaryotic cells have evolved an impressive array of DNA repair mechanisms that are able to detect and repair these lesions, thus preventing genomic instability. The DNA repair process is subjected to precise spatiotemporal coordination, and repair proteins are recruited to lesions in an orderly fashion, depending on their function. Here, we present DNArepairK, a unique open-access database that contains the kinetics of recruitment and removal of 70 fluorescently tagged DNA repair proteins to complex D

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Li, Y. F., L. M. Wen, J. Zhao, et al. "In Vitro and In Vivo Efficacy of DNA Damage Repair Inhibitor Veliparib in Combination with Artesunate against Echinococcus granulosus." Disease Markers 2020 (July 4, 2020): 1–11. http://dx.doi.org/10.1155/2020/8259820.

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Cystic echinococcosis (CE), caused by the cestode Echinococcus granulosus, is a worldwide chronic zoonosis. Albendazole (ABZ) and mebendazole are effective against CE, but a high dosage in a long-term period is usually required. In this study, we evaluate the effects of DNA damage repair inhibitor (i.e., Veliparib) in combination with artesunate (AS) on hydatid cysts. For the in vitro assay, protoscoleces of E. granulosus (E.g PSCs) were incubated with low AS (AS-L, 65 μM), moderate AS (AS-M, 130 μM), and high AS (AS-H, 325 μM), AS-L/M/H+Veliparib (10 μM), and ABZ (25 μM), respectively. The AS

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Faulhaber, Eva-Maria, Tina Jost, Julia Symank, et al. "Kinase Inhibitors of DNA-PK, ATM and ATR in Combination with Ionizing Radiation Can Increase Tumor Cell Death in HNSCC Cells While Sparing Normal Tissue Cells." Genes 12, no. 6 (2021): 925. http://dx.doi.org/10.3390/genes12060925.

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(1) Kinase inhibitors (KI) targeting components of the DNA damage repair pathway are a promising new type of drug. Combining them with ionizing radiation therapy (IR), which is commonly used for treatment of head and neck tumors, could improve tumor control, but could also increase negative side effects on surrounding normal tissue. (2) The effect of KI of the DDR (ATMi: AZD0156; ATRi: VE-822, dual DNA-PKi/mTORi: CC-115) in combination with IR on HPV-positive and HPV-negative HNSCC and healthy skin cells was analyzed. Cell death and cell cycle arrest were determined using flow cytometry. Addit

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Sutherland, May S. K., Changpu Yu, Christine O'Day, et al. "SGN-CD33A in Combination with Hypomethylating Agents Is Highly Efficacious in Preclinical Models of AML." Blood 126, no. 23 (2015): 3785. http://dx.doi.org/10.1182/blood.v126.23.3785.3785.

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Abstract Acute myeloid leukemia (AML) remains a therapeutic challenge. Long-term survival rates, in particular for older AML patients, remain poor, highlighting the need for improved and well-tolerated treatment options. AML patients who are unfit for high dose chemotherapy in the US are often prescribed hypomethylating agents (azacitidine or decitabine) although the efficacy of these agents in this population was modest (Estey, Leukemia 2013). SGN-CD33A is a CD33-directed antibody drug conjugate (ADC) that is comprised of a cysteine-engineered anti-CD33 antibody, a cleavable dipeptide linker

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Gallo, Adriana, Rosaria Landi, Valentina Rubino, et al. "Oxytetracycline induces DNA damage and epigenetic changes: a possible risk for human and animal health?" PeerJ 5 (April 27, 2017): e3236. http://dx.doi.org/10.7717/peerj.3236.

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Background Oxytetracycline (OTC), which is largely employed in zootechnical and veterinary practices to ensure wellness of farmed animals, is partially absorbed within the gastrointestinal tract depositing in several tissues. Therefore, the potential OTC toxicity is relevant when considering the putative risk derived by the entry and accumulation of such drug in human and pet food chain supply. Despite scientific literature highlights several OTC-dependent toxic effects on human and animal health, the molecular mechanisms of such toxicity are still poorly understood. Methods Here, we evaluated

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Lin, Chi-Kang, Shu-Ting Liu, Zih-Syuan Wu, Yu-Chi Wang, and Shih-Ming Huang. "Mechanisms of Cisplatin in Combination with Repurposed Drugs against Human Endometrial Carcinoma Cells." Life 11, no. 2 (2021): 160. http://dx.doi.org/10.3390/life11020160.

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Although endometrial carcinoma is one of the most common gynecological malignancies worldwide, its precise etiology remains unknown. Moreover, no novel adjuvant and/or targeted therapies are currently being developed to achieve greater efficacy for endometrial cancer patients who develop chemotherapeutic drug resistance. In this study, we used three human endometrial cancer cell lines, RL95-2, HEC-1-A, and KLE, to investigate the responsiveness of cisplatin alone and in combination with potential repurposed drugs. We first found that RL95-2 cells were more sensitive to cisplatin than HEC-1-A o

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Nair, Gopakumar Gopinathan, and Cherupally Krishnan Krishnan Nair. "Radioprotective Effects of Gallic Acid in Mice." BioMed Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/953079.

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Radioprotecting ability of the natural polyphenol, gallic acid (3,4,5-trihydroxybenzoic acid, GA), was investigated in Swiss albino mice. Oral administration of GA (100 mg/kg body weight), one hour prior to whole body gamma radiation exposure (2–8 Gy; 6 animals/group), reduced the radiation-induced cellular DNA damage in mouse peripheral blood leukocytes, bone marrow cells, and spleenocytes as revealed by comet assay. The GA administration also prevented the radiation-induced decrease in the levels of the antioxidant enzyme, glutathione peroxidise (GPx), and nonprotein thiol glutathione (GSH)

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Musiałek, Marcelina W., and Dorota Rybaczek. "Hydroxyurea—The Good, the Bad and the Ugly." Genes 12, no. 7 (2021): 1096. http://dx.doi.org/10.3390/genes12071096.

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Hydroxyurea (HU) is mostly referred to as an inhibitor of ribonucleotide reductase (RNR) and as the agent that is commonly used to arrest cells in the S-phase of the cycle by inducing replication stress. It is a well-known and widely used drug, one which has proved to be effective in treating chronic myeloproliferative disorders and which is considered a staple agent in sickle anemia therapy and—recently—a promising factor in preventing cognitive decline in Alzheimer’s disease. The reversibility of HU-induced replication inhibition also makes it a common laboratory ingredient used to synchroni

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Radcliffe, Colleen M., Elizabeth A. Silva, and Shelagh D. Campbell. "A method for assaying the sensitivity of Drosophila replication checkpoint mutants to anti-cancer and DNA-damaging drugs." Genome 45, no. 5 (2002): 881–89. http://dx.doi.org/10.1139/g02-051.

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In multi-cellular organisms, failure to properly regulate cell-cycle progression can result in inappropriate cell death or uncontrolled cell division leading to tumor formation. To guard against such events, conserved regulatory mechanisms called "checkpoints" block progression into mitosis in response to DNA damage and incomplete replication, as well as in response to other signals. Checkpoint mutants in organisms as diverse as yeast and humans are sensitive to various chemical agents that inhibit DNA replication or cause DNA damage. This phenomenon is the primary rationale for chemotherapy,

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Wang, Cun, Hui Wang, Cor Lieftink, et al. "CDK12 inhibition mediates DNA damage and is synergistic with sorafenib treatment in hepatocellular carcinoma." Gut 69, no. 4 (2019): 727–36. http://dx.doi.org/10.1136/gutjnl-2019-318506.

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ObjectivesHepatocellular carcinoma (HCC) is one of the most frequent malignancies and a major leading cause of cancer-related deaths worldwide. Several therapeutic options like sorafenib and regorafenib provide only modest survival benefit to patients with HCC. This study aims to identify novel druggable candidate genes for patients with HCC.DesignA non-biased CRISPR (clustered regularly interspaced short palindromic repeats) loss-of-function genetic screen targeting all known human kinases was performed to identify vulnerabilities of HCC cells. Whole-transcriptome sequencing (RNA-Seq) and bio

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Hao, Jianwen, Qizhen Peng, Keruo Wang, et al. "Antitumor Effect of Lenvatinib Combined with Alisertib in Hepatocellular Carcinoma by Targeting the DNA Damage Pathway." BioMed Research International 2021 (July 22, 2021): 1–13. http://dx.doi.org/10.1155/2021/6613439.

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Background and Aim. Although a strong antitumor effect of lenvatinib has been noted for patients with unresectable hepatocellular carcinoma (HCC), its efficacy requires improvement. It is imperative to seek therapeutic strategies that combine Lenvatinib with other anticancer agents. In this study, we investigated the anticancer effect of combining lenvatinib with alisertib, aurora A kinase (AURKA) target drug, against HCC in vitro and in vivo. Methods. Immunohistochemical staining, sequencing, and genetic analysis of liver cancer tissues were performed. The antitumor efficacy of single-agent o

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Morton, Lindsay M., Sarah L. Kerns, and M. Eileen Dolan. "Role of Germline Genetics in Identifying Survivors at Risk for Adverse Effects of Cancer Treatment." American Society of Clinical Oncology Educational Book, no. 38 (May 2018): 775–86. http://dx.doi.org/10.1200/edbk_201391.

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The growing population of cancer survivors often faces adverse effects of treatment, which have a substantial impact on morbidity and mortality. Although certain adverse effects are thought to have a significant heritable component, much work remains to be done to understand the role of germline genetic factors in the development of treatment-related toxicities. In this article, we review current understanding of genetic susceptibility to a range of adverse outcomes among cancer survivors (e.g., fibrosis, urinary and rectal toxicities, ototoxicity, chemotherapy-induced peripheral neuropathy, s

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Beyer, Mandy, Annette Romanski, Al-Hassan M. Mustafa та ін. "HDAC3 Activity is Essential for Human Leukemic Cell Growth and the Expression of β-catenin, MYC, and WT1". Cancers 11, № 10 (2019): 1436. http://dx.doi.org/10.3390/cancers11101436.

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Therapy of acute myeloid leukemia (AML) is unsatisfactory. Histone deacetylase inhibitors (HDACi) are active against leukemic cells in vitro and in vivo. Clinical data suggest further testing of such epigenetic drugs and to identify mechanisms and markers for their efficacy. Primary and permanent AML cells were screened for viability, replication stress/DNA damage, and regrowth capacities after single exposures to the clinically used pan-HDACi panobinostat (LBH589), the class I HDACi entinostat/romidepsin (MS-275/FK228), the HDAC3 inhibitor RGFP966, the HDAC6 inhibitor marbostat-100, the non-s

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Cao, Ji, Lei Zhang, Qing Ye, et al. "YQ36: A Novel Bisindolylmaleimide Analogue Induces KB/VCR Cell Death." Journal of Biomedicine and Biotechnology 2009 (2009): 1–11. http://dx.doi.org/10.1155/2009/535072.

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Overexpression of multidrug resistance proteins P-glycoprotein (P-gp, MDR1) causes resistance of the tumor cells against a variety of chemotherapeutic agents. 3-(1-methyl-1H-indol-3-yl)-1-phenyl-4-(1-(3-(piperidin-1-yl)propyl)-1H-pyrazolo[3,4-b]pyridine-3-yl)-1H-pyrrole-2,5-dione (YQ36) is a novel analogue of bisindolylmaleimide, which has been reported to overcome multidrug resistance. Here, we dedicated to investigate the anticancer activity of YQ36 on KB/VCR cells. The results revealed that YQ36 exhibited great antiproliferative activity on three parental cell lines and MDR1 overexpressed c

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Rojas, Marta, Colin W. Wright, Benjamin Piña, and José Portugal. "Genomewide Expression Profiling of Cryptolepine-Induced Toxicity in Saccharomyces cerevisiae." Antimicrobial Agents and Chemotherapy 52, no. 11 (2008): 3844–50. http://dx.doi.org/10.1128/aac.00532-08.

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ABSTRACT We have used the budding yeast Saccharomyces cerevisiae to identify genes that may confer sensitivity in vivo to the antimalarial and cytotoxic agent cryptolepine. Five S. cerevisiae strains, with different genetic backgrounds in cell permeability and DNA damage repair mechanisms, were exposed to several concentrations of cryptolepine. Cryptolepine showed a relatively mild toxicity for wild-type strains, which was augmented by either increasing cell permeability (Δerg6 or ISE2 strains) or disrupting DNA damage repair (Δrad52 strains). These results are compatible with the ability of c

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Cesar, Pedro H. S., Marcus V. C. Trento, Daniela A. Oliveira, Anderson A. Simão, Larissa F. A. Vieira, and Silvana Marcussi. "Prospection of Effects of Guava Leaves Infusion: Antigenotoxic Action and Enzymatic Inhibition." Natural Product Communications 12, no. 6 (2017): 1934578X1701200. http://dx.doi.org/10.1177/1934578x1701200631.

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Several forms of Psidium guajava L. (guava) leaf preparations have been widely used for prevention and treatment of illnesses. However, researches about the protective action of guava's natural products on the genetic material of animal cells is scarce. Accordingly, the aim of this study was to evaluate the antigenotoxic potential of infusions of guava leaves from three cultivars (Pedro Sato, Paluma and Roxa) against DNA damage induced by Doxorubicin (DXR) in human leukocytes, and their effects on enzymatic inhibition. To assess the antigenotoxic potential of these infusions, a comet assay (si

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Paterniti, Irene, Sarah Adriana Scuderi, Giovanna Casili, et al. "Poly (ADP-Ribose) Polymerase Inhibitor, ABT888, Improved Cisplatin Effect in Human Oral Cell Carcinoma." Biomedicines 9, no. 7 (2021): 771. http://dx.doi.org/10.3390/biomedicines9070771.

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Cisplatin is one of the chemotherapeutic drugs used for the management of oral carcinoma, in which combined therapies are estimated to exert superior therapeutic efficacy compared with monotherapy. It is known that poly(ADP-ribosyl)ation is implicated in a multiplicity of cellular activities, such as DNA repair and cell death. Based on these, PARP inhibitors are used for the treatment of cancers; however, the capacity of PARP inhibitors associated to anti-cancer drugs have not been completely assessed in oral carcinoma. Here, we evaluated the effects of PARPi veliparib (ABT888) in combination

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Ayers, Michael C., Zachary N. Sherman, and Jennifer E. G. Gallagher. "Oxidative Stress Responses and Nutrient Starvation in MCHM Treated Saccharomyces cerevisiae." G3: Genes|Genomes|Genetics 10, no. 12 (2020): 4665–78. http://dx.doi.org/10.1534/g3.120.401661.

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In 2014, the coal cleaning chemical 4-methylcyclohexane methanol (MCHM) spilled into the water supply for 300,000 West Virginians. Initial toxicology tests showed relatively mild results, but the underlying effects on cellular biology were underexplored. Treated wildtype yeast cells grew poorly, but there was only a small decrease in cell viability. Cell cycle analysis revealed an absence of cells in S phase within thirty minutes of treatment. Cells accumulated in G1 over a six-hour time course, indicating arrest instead of death. A genetic screen of the haploid knockout collection revealed 32

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Coyle, Thomas E., Alicia K. Bair, Constance Stein, Neerja Vajpayee, and Syed Mehdi. "Acute Leukemia Associated with Valproic Acid Treatment: A Novel Mechanism for Leukemogenesis?." Blood 104, no. 11 (2004): 4453. http://dx.doi.org/10.1182/blood.v104.11.4453.4453.

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Abstract Valproic acid (VA) is the most commonly used antiepileptic drug. It has a wide spectrum of hematologic toxicity including thrombocytopenia, anemia, leukopenia, macrocytosis and the presence of the Pelger-Huet abnormality. Serious but reversible hematologic toxicity resembling a myelodysplastic syndrome (MDS) has also been reported. In these cases, cytogenetics, when tested, was normal and progression to acute leukemia was not reported. We now report three cases of acute leukemia associated with VA therapy, accompanied by cytogenetic abnormalities and features suggestive of secondary l

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Cea, Michele, Antonia Cagnetta, Aditya Munshi, et al. "Compromised Nuclear Sirtuins Activity Sensitizes BRCA-Proficient multiple Myeloma Cells to DNA Damage Agents." Blood 120, no. 21 (2012): 723. http://dx.doi.org/10.1182/blood.v120.21.723.723.

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Abstract Abstract 723 Background: Multiple myeloma (MM) is a clonal malignancy of plasma cells with hallmark genetic instability resulting in large-scale changes at diagnosis, as well as further evolution contributing to disease progression. Inhibition of DNA repair mechanisms leads to significant reduction in acquisition of new genetic changes and associated progression of MM. Mammalian sirtuins are class III NAD+-dependent deacetylases emerging as innovative proteins involved in multiple pathways, including genome maintenance. Methods: A panel of 18 MM cell lines, both sensitive and resistan

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Lopes, Nair, Mariana Brütt Pacheco, Diana Soares-Fernandes, et al. "Hydralazine and Enzalutamide: Synergistic Partners against Prostate Cancer." Biomedicines 9, no. 8 (2021): 976. http://dx.doi.org/10.3390/biomedicines9080976.

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Advanced prostate cancers frequently develop resistance to androgen-deprivation therapy with serious implications for patient survival. Considering their importance in this type of neoplasia, epigenetic modifications have drawn attention as alternative treatment strategies. The aim of this study was to assess the antitumoral effects of the combination of hydralazine, a DNA methylation inhibitor, with enzalutamide, an antagonist of the androgen receptor, in prostate cancer cell lines. Several biological parameters, such as cell viability, proliferation, DNA damage, and apoptosis, as well as clo

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Mohamed, Magda F., Nada S. Ibrahim, Ahmed H. M. Elwahy, and Ismail A. Abdelhamid. "Molecular Studies on Novel Antitumor Bis 1,4-Dihydropyridine Derivatives Against Lung Carcinoma and their Limited Side Effects on Normal Melanocytes." Anti-Cancer Agents in Medicinal Chemistry 18, no. 15 (2019): 2156–68. http://dx.doi.org/10.2174/1871520618666181019095007.

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Background: Cancer is a complex genetic disease which is characterized by an abnormal cell growth, invasion and spreading to other parts of the body. There are several factors that lead to cancer by causing DNA damage and the impairment of its repair. Treatment of cancer using the chemotherapeutic drugs have adverse side effects such as toxicity as they lose their specificity toward cancer cells and affect also normal cells. Moreover, the cancer cells can resist the chemotherapeutic agents and make them ineffective. For these reasons, much attentions have been paid to develop new drugs with li

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Haghighitalab, Azadeh, Maryam M. Matin, Ahmad Reza Bahrami, Mehrdad Iranshahi, Morvarid Saeinasab, and Fereshteh Haghighi. "In vitro Investigation of Anticancer, Cell-Cycle-Inhibitory, and Apoptosis-Inducing Effects of Diversin, a Natural Prenylated Coumarin, on Bladder Carcinoma Cells." Zeitschrift für Naturforschung C 69, no. 3-4 (2014): 99–109. http://dx.doi.org/10.5560/znc.2013-0006.

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Chemotherapy is one of the main strategies for reducing the rate of cancer progression or, in some cases, curing the tumour. Since a great number of chemotherapeutic agents are cytotoxic compounds, i. e. similarly affect normal and neoplastic cells, application of antitumour drugs is preferred in cancer management and therapy. In this study, the cytotoxicity of diversin was evaluated in 5637 cells, a transitional cell carcinoma (TCC) subline (bladder carcinoma), and normal human fibroblast cells using the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Chromatin c

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Samuel, Priya, Laura Ann Mulcahy, Fiona Furlong, et al. "Cisplatin induces the release of extracellular vesicles from ovarian cancer cells that can induce invasiveness and drug resistance in bystander cells." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1737 (2017): 20170065. http://dx.doi.org/10.1098/rstb.2017.0065.

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Ovarian cancer has a poor overall survival that is partly caused by resistance to drugs such as cisplatin. Resistance can be acquired as a result of changes to the tumour or due to altered interactions within the tumour microenvironment. Extracellular vesicles (EVs), small lipid-bound vesicles that are loaded with macromolecular cargo and released by cells, are emerging as mediators of communication in the tumour microenvironment. We previously showed that EVs mediate the bystander effect, a phenomenon in which stressed cells can communicate with neighbouring naive cells leading to various eff

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Sweder, Kevin. "Recent advances in understanding/assessing toxicity to the epigenome." F1000Research 6 (February 1, 2017): 96. http://dx.doi.org/10.12688/f1000research.9649.1.

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The ability of non-genotoxic agents to induce cancer has been documented and clearly requires a reassessment of testing for environmental and human safety. Drug safety testing has historically relied on test batteries designed to detect DNA damage leading to mutation and cancer. The standard genetic toxicology testing battery has been a reliable tool set to identify small molecules/chemicals as hazards that could lead to genetic changes in organisms and induction of cancer. While pharmaceutical companies and regulatory agencies have extensively used the standard battery, it is not suitable for

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A, Abou-eisha, and Adel E. El-din. "GENOTOXIC AND CARCINOGENIC STUDIES OF NORGESTREL IN DROSOPHILA MELANOGASTER." Asian Journal of Pharmaceutical and Clinical Research 11, no. 10 (2018): 372. http://dx.doi.org/10.22159/ajpcr.2018.v11i10.27374.

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Objective: The aim of this study was to investigate, for the first time, the possible in vivo genotoxic and carcinogenic activity associated with exposure to norgestrel (NGT) drug through employing the very recently established and adjusted genotoxic and tumorigenic methods in Drosophila melanogaster.Methods: Two in vivo genotoxic test systems were used; one detects the somatic mutation and recombination effects (somatic mutation and recombination test [SMART] wing-spot test) and the other detects the primary DNA damage (the comet test) in the body cells of D. melanogaster. On the other hand,

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Nikoleousakos, Nikolaos, Panagiotis Dalezis, Aikaterini Polonifi, et al. "Cytocidal Antitumor Effects against Human Ovarian Cancer Cells Induced by B-Lactam Steroid Alkylators with Targeted Activity against Poly (ADP-Ribose) Polymerase (PARP) Enzymes in a Cell-Free Assay." Biomedicines 9, no. 8 (2021): 1028. http://dx.doi.org/10.3390/biomedicines9081028.

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We evaluated three newly synthesized B-lactam hybrid homo-aza-steroidal alkylators (ASA-A, ASA-B and ASA-C) for their PARP1/2 inhibition activity and their DNA damaging effect against human ovarian carcinoma cells. These agents are conjugated with an alkylating component (POPA), which also served as a reference molecule (positive control), and were tested against four human ovarian cell lines in vitro (UWB1.289 + BRCA1, UWB1.289, SKOV-3 and OVCAR-3). The studied compounds were thereafter compared to 3-AB, a known PARP inhibitor, as well as to Olaparib, a standard third-generation PARP inhibito

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He, Chuan Hua, and Dindial Ramotar. "An allele of the yeast RPB7 gene, encoding an essential subunit of RNA polymerase II, reduces cellular resistance to the antitumor drug bleomycin." Biochemistry and Cell Biology 77, no. 4 (1999): 375–82. http://dx.doi.org/10.1139/o99-039.

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Bleomycin is an antitumor drug that kills cells by introducing lesions in DNA. Thus, normal cells exposed to bleomycin must rely on efficient DNA repair mechanisms to survive. In the yeast Saccharomyces cerevisiae, the transcriptional activator Imp2 is required to fend off the toxic effects of bleomycin. However, it remains unclear whether Imp2 controls the expression of a protein that either repairs bleomycin-induced DNA lesions, or detoxifies the drug, and or both. To gain further insight into the mechanisms by which yeast cells mount a response towards bleomycin, we began to sequentially ch

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Juvik, John A. "Genetic Improvement of Vegetables for Enhanced Cancer Chemoprevention." HortScience 32, no. 3 (1997): 555D—555. http://dx.doi.org/10.21273/hortsci.32.3.555d.

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Extensive epidemiological evidence suggests that carotenoids (including vitamin A), ascorbate (vitamin C), tocols (including vitamin E), and glucosinolate breakdown products exert anticarcinogenic effects in a range of human tissues. Consumption of fresh and processed vegetables with enhanced levels of these phytochemicals could reduce human risk of cancer. The vitamins play a major role as antioxidants, offering protection against cancer by preventing or reversing oxidative damage to DNA and other cellular components. Cruciferous vegetables contain glucosinolates (GSs), which, during masticat

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Schoch, Sarah, Vasily Sen, Walburgis Brenner, Andrea Hartwig, and Beate Köberle. "In Vitro Nephrotoxicity Studies of Established and Experimental Platinum-Based Compounds." Biomedicines 9, no. 8 (2021): 1033. http://dx.doi.org/10.3390/biomedicines9081033.

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Cisplatin is one of the most commonly used drugs for the treatment of various solid cancers. However, its efficacy is restricted by severe side effects, especially dose-limiting nephrotoxicity. New platinum-based compounds are designed to overcome this limitation. Previous investigations showed that the platinum(IV)–nitroxyl complex PN149 is highly cytotoxic in various tumor cell lines. In the present study, investigations with PN149 were extended to normal human kidney tubule epithelia. Coincident with higher intracellular platinum accumulation, the cytotoxicity of PN149 in the proximal tubul

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Zhou, Changyin, Xue Zhang, Yuwei Zhang, et al. "Vitamin C protects carboplatin-exposed oocytes from meiotic failure." Molecular Human Reproduction 25, no. 10 (2019): 601–13. http://dx.doi.org/10.1093/molehr/gaz046.

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Abstract CBP (carboplatin) is a second-generation chemotherapeutic drug of platinum compound commonly applied in the treatment of sarcomas and germ cell tumours. Although it is developed to replace cisplatin, which has been proven to have a variety of side effects during cancer treatment, CBP still exhibits a certain degree of toxicity including neurotoxicity, nephrotoxicity, hematotoxicity and myelosuppression. However, the underlying mechanisms regarding how CBP influences the female reproductive system especially oocyte quality have not yet been fully determined. Here, we report that CBP ex

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Wang, Lili, Shanye Yin, Aina zurita Martinez, et al. "Integrated Genomic and Proteomic Analysis of Murine CLL-like Cells Reveals SF3B1 Mutation to Impact DNA Damage Response and BCR Signaling." Blood 132, Supplement 1 (2018): 947. http://dx.doi.org/10.1182/blood-2018-99-117691.

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Abstract Collective large-scale sequencing efforts have unexpectedly revealed the high frequency of mutations in the splicing factor genes (SF3B1, U2AF1, SRSF2, ZRSR2) in various solid and hematological cancers, suggesting the association of splicing dysregulation with tumorigenesis. Mutations in SF3B1 occur in 5-20% of patients with chronic lymphocytic leukemia (CLL) and are associated with poorer overall survival and chemotherapy resistance. These mutations are restricted to hotspots (>50% at K700E site) and strongly co-occur with ATM mutations (loss-of-function) and deletion of 11q (ATM

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